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Biomedical subjects

A F Ryan

Publications and source records attributed to A F Ryan.

138 records · Page 8Linked to original sources
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Histamine-induced middle ear effusion and mucosal histopathology in the guinea pig.

It has been suggested that immune responses and resultant generation or release of inflammatory mediators play a role in otitis media with effusion (OME). To explore the potential of one such mediator to contribute to OME, the effects of histamine injected into the middle ear cavity were examined. Injection of histamine into the guinea pig middle ear was found to produce dilation and endothelial disjunction in capillaries, leading to striking mucosal edema and effusion which persisted for at least several hours. This response could be partially blocked by pretreatment with either H1 or H2 antihistamines. It is suggested that histamine released during immune responses in the middle ear may contribute to the formation of effusion and submucosal edema as observed in OME.

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A reexamination of experimental type II collagen autoimmunity: middle and inner ear morphology and function.

Type II collagen autoimmunity has been reported to result in a number of middle and inner ear morphological and functional abnormalities. We investigated the immunological, electrophysiological, and anatomical effects of this autoimmune state in well-established Wistar-Furth rat models of type II collagen autoimmune arthritis. Seventeen animals immunized with bovine type II collagen were divided into short term (1-3 months postimmunization) and long term (9-11 months) groups. Thirty-three experimental ears were tested electrophysiologically and were compared to nine ears of unimmunized Wistar-Furth rats. No hearing loss was found in the immunized animals, except for four animals that showed middle ear abscess formation consistent with spontaneous, purulent otitis media. All immunized animals showed very significant serum and perilymph antibody titers to type II collagen. No morphological abnormalities of the external, middle, or inner ears could be identified in the noninfected experimental animals. These findings do not support previously reported observations that type II collagen autoimmunity results in ear disease.

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Secondary immune response in the middle ear: immunological, morphological, and physiological observations.

A model of secondary immune response in the middle ear (ME) was developed in the guinea pig. Animals were immunized intradermally with keyhole limpet hemocyanin (KLH) and challenged with KLH in the ME 8 weeks later. The ME displayed effusion, mucosal hyperplasia, mucosal edema, and leukocytic infiltration. These responses were maximal at 3 days postchallenge, and persisted for 2 to 3 weeks. High levels of antibody were observed in the ME effusions, and serum titers increased significantly. Immunohistochemical localization of antibody indicated that substantial free IgG was present in the submucosa, with much less in the mucosal epithelium. IgA plasma cells were observed in the submucosa at 1 week postchallenge, but no IgM was detected. In contrast to the response observed in sensitized animals, antigen presented to the ME of unimmunized control animals resulted in no effusion, minimal mucosal inflammation, and little or no antibody in either the ME or serum. However, substantial neutrophilic infiltration of the ME cavity was observed. The effusion and inflammation produced by secondary ME immune responses were not affected by tympanostomy tubes. Eustachian tube function as measured by a forced response test was not affected by ME immune response. This suggests that the immunologically induced effusion was not the result of eustachian tube obstruction. We postulate that increased vascular permeability in the ME mucosa, induced by chemical mediators, resulted in the transudation of serum.

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Potentiation of kanamycin ototoxicity by a history of noise exposure.

Chinchillas were exposed to a noise band (1,414 to 5,656 Hz, 100-dB sound pressure level [SPL] for one hour) and treated with kanamycin (150 mg/kg a day until hearings loss was noted at 6.0 kHz) either separately, simultaneously, or sequentially. Simultaneous noise and kanamycin resulted in interactive potentiation of threshold shift and cochlear pathologic condition. Kanamycin treatment two months after noise exposure produced similar potentiation. No interaction was seen when noise exposure occurred one month after kanamycin treatment.

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Audiometric and histologic correlates of the interaction between kanamycin and subtraumatic levels of noise in the chinchilla.

Difficulty in assessment of potentiating interaction between noise-induced and kanamycin-induced injury of hearing is compounded by the great variability of intersubject response to the same drug dosage. However, in a given subject, response of the two cochleas to kanamycin intoxication may resonably be assumed to be symmetric. The present study was designed to utilize this similarity, in determining whether kanamycin intoxication would potentiate a normally subtraumatic noise stimulus. Under the experimental conditions outlined, it was found that after a dosage of 150 mg/kg/day of kanamycin given to a physiologic end point, normally subtraumatic noise caused consistent increas in hearing loss.

Acoustic Stimulation↗
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Element content of intracochlear fluids, outer hair cells, and stria vascularis as determined by energy-dispersive roentgen ray analysis.

Roentgen ray spectrometry was used to obtain element spectra from isolated samples of perilymph, endolymph, outer hair cells, and stria vascularis obtained by microdissection from the freeze-dried inner ears of chinchillas. The spectra of perilymph and endolymph residues indicated that no cross-contamination of the two cochlear fluids occurs during freeze-drying or sampling. The spectra of outer hair cells suggested that the extracellular fluid in the organ of Corti spaces is similar to perilymph in its ionic content. The spectra of stria vascularis samples indicated low sodium and high phosphorus contents. Energy-dispersive roentgen ray analysis of freeze-dried inner ears appears to be a promising method for low-contamination measurement of ion distribution in the cochlea.

Animals↗
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Passive transfer of immune-mediated middle ear inflammation and effusion.

Antigenic challenge in the middle ear of animals previously sensitized intradermally results in an immunologically mediated inflammatory response, including the generation of serous effusion in the middle ear cavity. The mechanisms which contribute to this immune-mediated otitis media with effusion (OME) were investigated by passive transfer with either purified IgG or with sensitized lymphocytes. A peritoneal exudate was raised in strain 13 guinea pigs by repeated injection of keyhole limpet hemocyanin (KLH) with complete Freund's adjuvant. IgG and lymphocytes were isolated from exudates and used for passive sensitization. Middle ear challenge following passive transfer of IgG specific to KLH produced effusion and inflammation which was equivalent to that observed in actively immunized animals, but resulted in significantly greater numbers of leukocytes infiltrating the middle ear. Unlike in the active response, few of the cells infiltrating the middle ear mucosa and middle ear cavity were eosinophils. Middle ear challenge with KLH following passive transfer with sensitized lymphocytes produced no middle ear effusion, relatively little mucosal inflammation, and sharply reduced exocytosis of leukocytes into the middle ear when compared with the active immune response or even with unimmunized controls. It is concluded that middle ear effusion, inflammation, and leukocytic exocytosis are mediated primarily by the IgG fraction of humoral immunity in our model of immune OME.

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Changes in cochlear blood flow during acoustic stimulation as determined by 14C-iodoantipyrine autoradiography.

Local blood flow was measured in the tissues of the cochlea using the [14C]iodoantipyrine autoradiographic technique. Flow observed without acoustic stimulation was compared with that seen during exposure to wide-band noise at 85 or 105 dB SPL. Compared with the unexposed cochlea, substantial increases in blood flow were observed during exposure to 85 dB SPL noise in the spiral ganglion, VIII nerve and spiral lamina. Little or no change was noted in external wall structures. These results are consistent with changes in cochlear metabolism which have been reported previously using similar techniques, suggesting that increases in blood flow may be linked to increases in local metabolism. No changes in blood flow were measured during exposure to 105 dB SPL noise. This result is similar to those of other investigators using potentially damaging intensities of acoustic stimulation.

Acoustic Stimulation↗
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Lymphocyte circulation to the middle ear.

The movement of lymphocytes into the tympanic cavity was studied during an immune response in the middle ear. Sensitized lymphocytes obtained from peripheral blood, peripheral lymph nodes, spleen, mesenteric lymph nodes and Peyer's patches of strain-13 inbred guinea pigs were labelled with 51Cr and injected intravenously into strain-13 recipients undergoing a middle ear immune response. The middle ears and immune organs of the recipients were assayed for radioactivity to detect the infiltration of labelled cells. Lymphocytes from all sources entered the middle ear mucosa in response to immune stimulation at equal levels, suggesting that the middle ear is seeded non-specifically by circulating lymphocytes in response to antigenic stimulation. The infiltration of lymphocytes of mucosal origin into the middle ear cavity is consistent with the participation of the middle ear in a defense system in common with other mucosal organs.

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Hearing loss in experimental cytomegalovirus infection of the guinea pig inner ear: prevention by systemic immunity.

Guinea pig cytomegalovirus (GPCMV) has been used to establish a reproducible model of viral labyrinthitis and hearing loss. Cochlear function was assessed by electrophysiological recordings of cochlear microphonic (CM) and eighth nerve N1 compound action potential (AP) thresholds prior to and up to eight days following inoculation of the scala tympani. Inner ear inoculation of seronegative subjects with live GPCMV produced profound elevations in CM and AP thresholds: 70% of these subjects had their thresholds raised to the limits of the sound system throughout the tested frequency range of 0.10 to 32 kHz. Histopathologic effects associated with CM and AP threshold shifts were primarily limited to the perilabyrinthine compartment, and were greatest in the most basal cochlear turns. Systemic infection with GPCMV produced an immune response, but did not affect CM or AP thresholds. Subsequent inoculation of the inner ear of these seropositive animals with live GPCMV did not result in either CM or AP threshold shifts, or cochlear histopathology. Inoculations of inactivated virus into the inner ears of seronegative and seropositive animals produced only moderate CM and AP threshold effects. Primary GPCMV labyrinthitis thus results in significant cochlear dysfunction and histopathologic changes which are prevented by prior systemic infection with GPCMV.

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